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Molecular Research of Gastrointestinal Disease 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 April 2025 | Viewed by 5192

Special Issue Editors


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Guest Editor
1. Institute for Health and Sport, Victoria University, Melbourne 3011, Australia
2. Department of Medicine Western Health, University of Melbourne, Melbourne 3010, Australia
3. Regenerative Medicine and Stem Cells Program, Australian Institute of Musculoskeletal Sciences, Melbourne 3021, Australia
Interests: development of novel therapies for the treatment of enteric neuropathy; gut–brain axis; inflammatory bowel disease; colorectal cancer; gastrointestinal side effects of chemotherapy
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Guest Editor
1. Institute for Health and Sport, Victoria University, Melbourne 3011, Australia
2. Research and Ethics Department, Goulburn Valley Health, Shepparton 3630, Australia
3. School of Rural Health, La Trobe University, Mildura 3520, Australia
Interests: enteric nervous system; mesenchymal stem-cell-based treatments; inflammatory bowel disease; enteric neuropathy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Recent technological advances unravel many molecular, cellular, genetic, immunological, and microbiological aspects of the gastrointestinal tract functions in health and disease. These discoveries have important implications for a better understanding of basic mechanisms that maintain the physiological homeostasis of the gut. Malfunctioning of these fine-tuned molecular mechanisms leads to the onset and progression of gastrointestinal disorders. Understanding the molecular mechanisms and pathways is the turning point toward the development of novel diagnostic approaches and therapies for gastrointestinal disorders. Led by Prof Kulmira Nurgali and Dr Ainsley Robinson and assisted by our promotion editor, Dr Nyanbol Kuol (University of Nevada, Reno, US), this Special Issue of IJMS, “Molecular Research of Gastrointestinal Disease 2.0”, welcomes basic and clinical original research and review papers to be submitted for peer review. The submitted papers can cover any aspects of molecular research relevant to a broad range of gastrointestinal disorders.

Topics of interest include but are not limited to: 

  • molecular mechanisms of gastrointestinal functions in health and disease;
  • molecular targets for therapeutic intervention;
  • molecular markers for diagnostics of gastrointestinal disorders.

Dr. Kulmira Nurgali
Dr. Ainsley Robinson
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • gastrointestinal health
  • gastrointestinal disorders
  • gastrointestinal disease
  • gastrointestinal homeostasis
  • molecular targets
  • mechanisms
  • pathways
  • molecular markers
  • therapeutic targets

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Related Special Issue

Published Papers (5 papers)

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Research

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15 pages, 7039 KiB  
Article
Rectal Epithelial Stem Cell Kinetics in Acute Radiation Proctitis
by Sharmila Ghosh, Akinori Morita, Yuichi Nishiyama, Masahiro Sakaue, Ken Fujiwara, Daiki Morita, Yuichiro Sonoyama, Yuichi Higashi and Megumi Sasatani
Int. J. Mol. Sci. 2024, 25(20), 11252; https://doi.org/10.3390/ijms252011252 - 19 Oct 2024
Viewed by 345
Abstract
The intestinal tract is a typical radiosensitive tissue, and radiation rectal injury is a severe side effect that limits the prescribed dose in radiotherapy of the abdominal and pelvic region. Understanding the post-irradiation kinetics of Lgr5-positive stem cells is crucial in comprehending [...] Read more.
The intestinal tract is a typical radiosensitive tissue, and radiation rectal injury is a severe side effect that limits the prescribed dose in radiotherapy of the abdominal and pelvic region. Understanding the post-irradiation kinetics of Lgr5-positive stem cells is crucial in comprehending this adverse process. In this study, we utilized Lgr5-EGFP knock-in mice expressing EGFP and LGR5 antibody fluorescence staining of wild-type mice. At the state of radiation injury, the qPCR analysis showed a significant decrease in the expression level of Lgr5 in the rectal epithelial tissue. The dose-response relationship analysis showed that at low to moderate doses up to 10 gray (Gy), Lgr5-clustered populations were observed at the base of the crypt, whereas at sublethal doses (20 Gy and 29 Gy), the cells exhibited a dot-like scatter pattern, termed Lgr5-dotted populations. During recovery, 30 days post-irradiation, Lgr5-clustered populations gradually re-emerged while Lgr5-dotted populations declined, implying that some of the Lgr5-dotted stem cell populations re-clustered, aiding regenerations. Based on statistical analysis of the dose-response relationship using wild-type mice, the threshold dose for destroying these stem cell structures is 18 Gy. These findings may help set doses in mouse abdominal irradiation experiments for radiation intestinal injury and for understanding the histological process of injury development. Full article
(This article belongs to the Special Issue Molecular Research of Gastrointestinal Disease 2.0)
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18 pages, 7117 KiB  
Article
Serotonin Transporter Deficiency Induces Metabolic Alterations in the Ileal Mucosa
by Nathan Calzadilla, Dulari Jayawardena, Aisha Qazi, Anchal Sharma, Kai Mongan, Shane Comiskey, Abhijith Eathara, Seema Saksena, Pradeep K. Dudeja, Waddah A. Alrefai and Ravinder K. Gill
Int. J. Mol. Sci. 2024, 25(8), 4459; https://doi.org/10.3390/ijms25084459 - 18 Apr 2024
Viewed by 1117
Abstract
Serotonin transporter (SERT) deficiency has been implicated in metabolic syndrome, intestinal inflammation, and microbial dysbiosis. Interestingly, changes in microbiome metabolic capacity and several alterations in host gene expression, including lipid metabolism, were previously observed in SERT−/− mice ileal mucosa. However, the precise [...] Read more.
Serotonin transporter (SERT) deficiency has been implicated in metabolic syndrome, intestinal inflammation, and microbial dysbiosis. Interestingly, changes in microbiome metabolic capacity and several alterations in host gene expression, including lipid metabolism, were previously observed in SERT−/− mice ileal mucosa. However, the precise host or microbial metabolites altered by SERT deficiency that may contribute to the pleiotropic phenotype of SERT KO mice are not yet understood. This study investigated the hypothesis that SERT deficiency impacts lipid and microbial metabolite abundances in the ileal mucosa, where SERT is highly expressed. Ileal mucosal metabolomics was performed by Metabolon on wild-type (WT) and homozygous SERT knockout (KO) mice. Fluorescent-activated cell sorting (FACS) was utilized to measure immune cell populations in ileal lamina propria to assess immunomodulatory effects caused by SERT deficiency. SERT KO mice exhibited a unique ileal mucosal metabolomic signature, with the most differentially altered metabolites being lipids. Such changes included increased diacylglycerols and decreased monoacylglycerols in the ileal mucosa of SERT KO mice compared to WT mice. Further, the ileal mucosa of SERT KO mice exhibited several changes in microbial-related metabolites known to play roles in intestinal inflammation and insulin resistance. SERT KO mice also had a significant reduction in the abundance of ileal group 3 innate lymphoid cells (ILC3). In conclusion, SERT deficiency induces complex alterations in the ileal mucosal environment, indicating potential links between serotonergic signaling, gut microbiota, mucosal immunity, intestinal inflammation, and metabolic syndrome. Full article
(This article belongs to the Special Issue Molecular Research of Gastrointestinal Disease 2.0)
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Review

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11 pages, 1746 KiB  
Review
The AP-2 Family of Transcription Factors—Still Undervalued Regulators in Gastroenterological Disorders
by Yi-Jin Yu, Damian Kołat, Żaneta Kałuzińska-Kołat, Zhu Liang, Bo-Qiang Peng, Yun-Feng Zhu, Kai Liu, Jia-Xin Mei, Gang Yu, Wei-Han Zhang, Xiao-Long Chen, Kun Yang, Jian-Kun Hu and Lin-Yong Zhao
Int. J. Mol. Sci. 2024, 25(17), 9138; https://doi.org/10.3390/ijms25179138 - 23 Aug 2024
Viewed by 750
Abstract
Activating enhancer-binding protein 2 (AP-2) is a family of transcription factors (TFs) that play crucial roles in regulating embryonic and oncogenic development. In addition to splice isoforms, five major family members encoded by the TFAP2A/B/C/D/E genes have been identified in humans, i.e., AP-2α/β/γ/δ/ε. [...] Read more.
Activating enhancer-binding protein 2 (AP-2) is a family of transcription factors (TFs) that play crucial roles in regulating embryonic and oncogenic development. In addition to splice isoforms, five major family members encoded by the TFAP2A/B/C/D/E genes have been identified in humans, i.e., AP-2α/β/γ/δ/ε. In general, the first three TFs have been studied more thoroughly than AP-2δ or AP-2ε. Currently, there is a relatively limited body of literature focusing on the AP-2 family in the context of gastroenterological research, and a comprehensive overview of the existing knowledge and recommendations for further research directions is lacking. Herein, we have collected available gastroenterological data on AP-2 TFs, discussed the latest medical applications of each family member, and proposed potential future directions. Research on AP-2 in gastrointestinal tumors has predominantly been focused on the two best-described family members, AP-2α and AP-2γ. Surprisingly, research in the past decade has highlighted the importance of AP-2ε in the drug resistance of gastric cancer (GC) and colorectal cancer (CRC). While numerous questions about gastroenterological disorders await elucidation, the available data undoubtedly open avenues for anti-cancer targeted therapy and overcoming chemotherapy resistance. In addition to gastrointestinal cancers, AP-2 family members (primarily AP-2β and marginally AP-2γ) have been associated with other health issues such as obesity, type 2 diabetes, liver dysfunction, and pseudo-obstruction. On the other hand, AP-2δ has been poorly investigated in gastroenterological disorders, necessitating further research to delineate its role. In conclusion, despite the limited attention given to AP-2 in gastroenterology research, pivotal functions of these transcription factors have started to emerge and warrant further exploration in the future. Full article
(This article belongs to the Special Issue Molecular Research of Gastrointestinal Disease 2.0)
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15 pages, 5325 KiB  
Review
What Happens in the Gut during the Formation of Neonatal Jaundice—Underhand Manipulation of Gut Microbiota?
by Hongfei Su, Shuran Yang, Shijing Chen, Xiaolin Chen, Mingzhang Guo, Longjiao Zhu, Wentao Xu and Huilin Liu
Int. J. Mol. Sci. 2024, 25(16), 8582; https://doi.org/10.3390/ijms25168582 - 6 Aug 2024
Cited by 1 | Viewed by 1235
Abstract
Jaundice is a symptom of high blood bilirubin levels affecting about 80% of neonates. In neonates fed with breast milk, jaundice is particularly prevalent and severe, which is likely multifactorial. With the development of genomics and metagenomics, a deeper understanding of the neonatal [...] Read more.
Jaundice is a symptom of high blood bilirubin levels affecting about 80% of neonates. In neonates fed with breast milk, jaundice is particularly prevalent and severe, which is likely multifactorial. With the development of genomics and metagenomics, a deeper understanding of the neonatal gut microbiota has been achieved. We find there are accumulating evidence to indicate the importance of the gut microbiota in the mechanism of jaundice. In this paper, we present new comprehensive insight into the relationship between the microbiota and jaundice. In the new perspective, the gut is a crucial crossroad of bilirubin excretion, and bacteria colonizing the gut could play different roles in the excretion of bilirubin, including Escherichia coli as the main traffic jam causers, some Clostridium and Bacteroides strains as the traffic police, and most probiotic Bifidobacterium and Lactobacillus strains as bystanders with no effect or only a secondary indirect effect on the metabolism of bilirubin. This insight could explain why breast milk jaundice causes a longer duration of blood bilirubin and why most probiotics have limited effects on neonatal jaundice. With the encouragement of breastmilk feeding, our perspective could guide the development of new therapy methods to prevent this side effect of breastfeeding. Full article
(This article belongs to the Special Issue Molecular Research of Gastrointestinal Disease 2.0)
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Other

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8 pages, 2173 KiB  
Case Report
Plexiform Fibromyxoma in the Stomach: Immunohistochemical Profile and Comprehensive Genetic Characterization
by Annabella Di Mauro, Rosalia Anna Rega, Maddalena Leongito, Vittorio Albino, Raffaele Palaia, Alberto Gualandi, Andrea Belli, Imma D’Arbitrio, Pasquale Moccia, Salvatore Tafuto, Annarosaria De Chiara, Alessandro Ottaiano and Gerardo Ferrara
Int. J. Mol. Sci. 2024, 25(9), 4847; https://doi.org/10.3390/ijms25094847 - 29 Apr 2024
Viewed by 1035
Abstract
Plexiform fibromyxoma (PF), also referred to as plexiform angiomyxoid myofibroblast tumor, is an exceedingly rare mesenchymal neoplasm primarily affecting the stomach. Herein, we present a case of PF diagnosed in a 71-year-old male with a history of lung cancer, initially suspected to have [...] Read more.
Plexiform fibromyxoma (PF), also referred to as plexiform angiomyxoid myofibroblast tumor, is an exceedingly rare mesenchymal neoplasm primarily affecting the stomach. Herein, we present a case of PF diagnosed in a 71-year-old male with a history of lung cancer, initially suspected to have a gastrointestinal stromal tumor (GIST) of the stomach, who subsequently underwent subtotal gastrectomy. The histopathological and molecular features of the tumor, including mutations in ABL1, CCND1, CSF1R, FGFR4, KDR, and MALAT1-GLI1 fusion, are elucidated and discussed in the context of diagnostic, prognostic, and therapeutic considerations. Full article
(This article belongs to the Special Issue Molecular Research of Gastrointestinal Disease 2.0)
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